The overall objective of this research program is to determine the effects of psychological stress on lipoprotein metabolism. This line of inquiry is being pursued because although stress and physiological responses to stressful environmental stimuli have been linked to the development of cardiovascular disease, no mechanism to account for this effect has been identified. Specifically, this research is proposed to: (a) determine the effects of acute laboratory stressors and epinephrine infusion on lipids, lipoproteins, and apoproteins B and A-I; (b) assess concurrent changes in heart rate, blood pressure, plasma catecholamines, and cortisol; (c) observe the time course over which stress- or epinephrine-induced changes in these various plasma constituents occur; and (d) determine whether individuals with eledvated plasma lipids exhibit greater lipoprotein responses to stress than those within the normolipidemic range. In the first study, 20 hyperlipidemics and 20 normolipidemics will be studied in the laboratory on 2 separate days. On one day, subjects will be presented with two stressful tasks, each lasting an hour. Lipoproteins, blood pressure, heart rate, catecholamines, and cortisol will be measured throughout the tasks and for 4 hours following administration of the tasks. On the second day, subjects will be monitored at rest for a comparable 6 hour period. Plasma lipoprotein differences between the control day and experimental day are predicted. During the second study, which has a design similar to that of the first study, 20 normolipidemic and 20 hyperlipidemic subjects will again be tested on a control day and during an experimental day. On the experimental day, dubjects will receive a 2-hour infusion of epinephrine, with lipoproteins, blood pressure, heart rate, catecholamines, and cortisol monitored throughout the infusion period and for 4 hours afterward. On the control day, subjects will be monitored throughout this time period, but no stressors or catecholamine infusions will be given. It is expected that the outcome of these investigations will shed some light on the mechanisms linking stress to coronary heart disease, and facilitate the development of a model to account for changes seen in lipoprotein metabolism as a function of stress.